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Matches in Nanopublications for { ?s ?p ?o <http://www.tkuhn.ch/bel2nanopub/RAe1bq-ZnDMl2apBFQmO3E-ViqIMReQkGXIKPRD0_1JFw#provenance>. }

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_6 label "Selventa" provenance.
_5 value "There is evidence that FANCD2,like BRCA1, participates in the events that are triggered by DNA damage during S and G2 phases and that lead to cell-cycle arrest. As well as modifying BRCA1, the ATM protein kinase can phosphorylate FANCD2 on several residues, including serine 222, following exposure to ionizing radiation77. Ser222 phosphorylation is required for the intra-S-phase arrest and is, in turn, dependent on the protein kinase NBS1, which is a component of the trimeric MRE11-RAD50-NBS1 complex78. FANCD2 can also be phosphorylated in an ATM-independent manner by the ATR kinase79,which signals an intra-S-phase arrest that is triggered by ultraviolet radiation or DNA-crosslinking agents46.Here, too, FANCD2 phosphorylation depends on NBS1, which is required to fully enforce the S-phase checkpoint. The participation of FANCD2 in ionizingradiation- activated checkpoint responses through phosphorylation on Ser222 seems to be independent78 of its mono-ubiquitylation on Lys561, which promotes the translocation of FANCD2 to damage-induced nuclear foci that contain BRCA1 and RAD51, and that are presumed sites of DNA repair. Similarly, FANCD2 foci do not require ATR-dependent phosphorylation79." provenance.
_5 wasQuotedFrom 15057286 provenance.
assertion hadPrimarySource 15057286 provenance.
large_corpus.bel title "BEL Framework Large Corpus Document" provenance.
large_corpus.bel description "Approximately 61,000 statements." provenance.
assertion wasDerivedFrom large_corpus.bel provenance.
assertion wasDerivedFrom _5 provenance.
large_corpus.bel authoredBy _6 provenance.
large_corpus.bel version "1.4" provenance.